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Burn Management in Orthopaedic Trauma A Critical Analysis Review Saad M. AlQahtani, MD, MSc(C) Mohammad M. Alzahrani, MD, MSc(C) Alberto Carli, MD, MSc Edward J. Harvey, MD, MSc, FRCSC
Investigation performed at the Division of Orthopaedic Surgery, Department of Surgery, McGill University Health Center, Montreal, Quebec, Canada
» The initial care of burn patients follows principles from the Advanced Trauma Life Support (ATLS) protocol with an emphasis on the ABCs (airway, breathing, and circulation) and adequate fluid resuscitation and with special attention to signs of smoke inhalation and carbon monoxide poisoning. The burn itself should be evaluated for extent (percent of total body surface area) and depth (grade) and should not distract from implementing an adequate ATLS protocol. » Electrical, circumferential, and full-thickness burns all are associated with an elevated risk of compartment syndrome. Prompt escharotomy or fasciotomy should be performed if patients exhibit increasing analgesic requirements or have elevated compartment pressures. » The historical standard of care for the treatment of fractures in association with burns has been external fixation. More recent data suggest that if patients are adequately resuscitated and stable, internal fixation of orthopaedic injuries within the first forty-eight hours after injury is associated with improved healing rates and a lower incidence of infection. Surgical incisions can be safely extended into burnt tissue to provide adequate operative exposure and fracture reduction. » Joint contracture is often a complication associated with burns, and patients with joint contracture as a consequence of being burned will often present to an orthopaedist for treatment. The optimal method to treat joint contractures in burn patients is to take a preventative approach that includes the provision of adequate analgesia, early active range-of-motion exercises, and timely plastic surgery consultation with regard to the excision of scar tissue. » Heterotopic ossification occurs in as much as 3% of burn patients and is not dependent on the location of the burn. Patients with heterotopic ossification are often referred to orthopaedists for treatment. Early active range-of-motion exercises, manipulation while the patient is under anesthesia, and delayed surgical resection are treatment options, but the overall risk for recurrence is high. In general, surgical excision of heterotopic bone is effective, but, to minimize the rate of recurrence, excision should be delayed until twelve months or more after injury, when maturation is complete. Neurovascular integration
COPYRIGHT © 2014 BY THE JOURNAL OF BONE AND JOINT SURGERY, INCORPORATED
JBJS REVIEWS 2014;2(10) :e4
Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. None of the authors, or their institution(s), have had any financial relationship, in the thirty-six months prior to submission of this work, with any entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. Also, no author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.
· http://dx.doi.org/10.2106/JBJS.RVW.N.00010
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within the heterotopic bone is common; therefore, preoperative computed tomography (CT) or magnetic resonance imaging (MRI) is indicated to plan safe excision of mature heterotopic bone.
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ach year, there are approximately 1.25 million burn patients seen in U.S. emergency rooms and more than 6000 hospital admissions1,2. Patients with burns often have associated skeletal injuries (10% in civilian populations and 24% in military populations)3,4. For civilians, the two most common mechanisms for orthopaedic injuries are motor-vehicle collisions and falls associated with electrical injury4-6. Treating burn patients who also have musculoskeletal injuries is a challenging task for orthopaedic surgeons. Timely soft-tissue management, adequate fluid resuscitation, prevention of infection, and concerns for long-term tissue coverage and joint function represent some of the topics that are pertinent to this unique subset of trauma patients. Thus, treatment of the burn and the orthopaedic injury as separate entities is not advised7, and regular coordination with emergency room physicians and plastic surgeons is recommended8. Fracture care in burn patients over the course of the past fifty years has evolved from a conservative stance (involving splinting, traction, and external fixation)9-11 to a more aggressive intervention (involving internal fixation and prompt, definitive soft-tissue management)5. The traditional treatment of fractures associated with burns has been external fixation (to achieve skeletal stability and alignment while maintaining access to the skin) and the avoidance of soft-tissue dissection (to minimize the risk of infection). More recent data suggest that, in selected patients, early internal fixation may achieve superior results with acceptable low rates of infection. Although the primary goal of orthopaedic management in these patients continues to be provisional skeletal stabilization, early operative intervention has been
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found to improve patient mobility, permit easier burn wound management, and decrease overall morbidity3,5,12. Burn injuries rank within the top fifteen leading causes of the burden of disease
TABLE I
globally13,14, yet guidelines for management of such injuries and their associated musculoskeletal manifestations are practically nonexistent within the orthopaedic literature. Complications that occur in patients with fractures associated with burns include infection, nonhealing incisions, delayed union, nonunion, stiffness, and scar formation.
ATLS Protocol for Evaluation and Treatment of Burn Patients*
Remove source of heat Remove all clothing and jewelry Cool burned area (if within first 3 hr after injury) with cold tap water for 30 min, then dry Cover patient with a sheet and apply burn shield for 24 hr Airway Assess Endotracheal large bore intubation if Unconscious Hypoxic with smoke inhalation Flash burns to the face or neck Identify signs of smoke inhalation, including Pharyngeal burn Air hunger Stridor Carbonaceous sputum Hoarseness Soot at the nares or mouth Provide oxygen for 24 hr Identify signs of carbon monoxide poisoning, including: Restlessness Headache Nausea Incoordination Memory loss Disorientation Coma Pinkish hue to skin Measure carboxyhemoglobin blood level Treat with 100% oxygen Circulation Assess peripheral pulses and heart beat Identify and stop sources of external bleeding (rarely caused by burns) Identify and stop sources of internal bleeding Urinary bladder (Foley) catheter Maintain urine output at 0.5 mL/kg/hr or 30 to 50 mL/hr *ATLS = Advanced Trauma Life Support.
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Fig. 1 Fig. 1A Schematic showing the three major layers of the skin and their involvement in various degrees of burn depth. First-degree burns are confined solely to the epidermis. Second-degree burns involve the epidermis and superficial dermis. Third-degree burns are full thickness through the epidermis and entire dermis. Fourth-degree burns extend the injury to the underlying structures, including muscle, tendon, and bone. (Illustration courtesy of Amicus Visual Solutions, Richmond, Virginia. Reproduced with permission.) Fig. 1B Chart showing natural history of burn degrees and typical treatment.
The purpose of this review is to (1) summarize the pathophysiology, classification, and initial evaluation of burns in burn patients who also have orthopaedic injuries; (2) provide evidence-based principles of fracture care, including antibiotic prophylaxis, soft-tissue handling, and nonoperative versus operative management; and (3) provide evidence-based recommendations for the treatment of chronic orthopaedic complications in burn patients. Anatomy and Pathophysiology Human skin is a complex and dynamic organ that provides a protective barrier against the surrounding environment. The major layers of skin are
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interdependent, functional units that can be divided into three identifiable layers (Fig. 1, A): the epidermis, the dermis, and the subcutaneous tissue layer. The epidermis is the thin outer layer of the skin, which is continuously shed and prevents the entry of microorganisms. The underlying dermis is composed mostly of type-I and typeIII collagen and provides skin with its elastic properties. The dermis also contains blood vessels, hair follicles, sweat glands, and sensory nerve fibers. The subcutaneous layer is the deepest layer of skin and primarily conserves body heat and dissipates external forces.
Local Effects of Burns The pathophysiology of the local and systemic response to thermal injury is understood. Increased skin temperature produces intracellular protein denaturation and the activation of toxic inflammatory mediators. These mediators promote vasoconstriction, disrupt the integrity of osmotic pressure gradients, and increase vascular permeability, leading to local perfusion changes and fluid shifts15. Complement and neutrophil activation lead to the development of cytotoxic oxygen free radicals, which directly damage surrounding tissue16. The temperature and duration of exposure determine the extent of local soft-tissue destruction. This
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Fig. 2 Fig. 2A Schematic demonstrating the zones of injury found within a burn. The zone of coagulation pertains to tissue that is irreversibly lost. The zone of stasis involves tissue that is potentially salvageable with appropriate perfusion and wound care. The zone of hyperemia contains viable tissue that is likely to survive. Fig. 2B Clinical photograph of the hand of a patient who sustained a flame-induced third-degree burn to the dorsal aspect of the left upper extremity. The patient underwent acute operative irrigation and debridement of nonviable tissue. The burned area was covered with a splitthickness skin graft and healed with good functional outcome.
local response was divided into threedimensional zones by Jackson in 1953 (Fig. 2, A)17. The area of maximum damage is referred to as the zone of coagulation and comprises irreversible tissue loss, absence of circulation, and coagulation of both intracellular and extracellular proteins. The surrounding zone of stasis is characterized by decreased but potentially salvageable, perfused tissue. Preservation of the zone of stasis through management of edema, infection, and hypotension is desired in burn management. The zone of stasis is surrounded by the zone of hyperemia, which is relatively uninjured by the burn itself but exhibits increased tissue perfusion from the physiological response to the burn injury and often recovers in the absence of severe sepsis or prolonged systemic hypoperfusion. Systemic Effects of Burns Burn injuries have been shown to produce systemic effects, including sympathetic stimulation, hypovolemia, renal failure, and myocardial dysfunction18-20. Such effects are referred to as burn shock and are
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common in burns that involve .30% of the total body surface area21. Burn shock occurs due to the interplay ofsoft-tissueloss, hypovolemia, and systemic mediators and persists as a dangerous pathophysiologic state even after fluid resuscitation has been initiated and hypovolemia is corrected22. If left untreated, this state leads to adult respiratory distress syndrome and progressive organdysfunction. Death is a risk with burn injuries, especially when such injuries involve .30% of the total body surface area. Classification of Burns Burns have historically been classified by their type and depth. Flash and flame burns are the most common cause of hospital admission for burn patients (Fig. 2, B)21, as these types of burns are often full-thickness and may be associated with inhalational injury and concomitant trauma. Scald burns are the most common cause of pediatric burn admissions and have been associated with up to 25% of nonaccidental childhood injuries23. These types of burns are generally deep partial thickness (second-degree burn) or full thickness
(third-degree burn) in depth24. Electrical burns from high-voltage sources are unique in that they cause extensive tissue injury at the entry point, the exit point, and the deeper structures in between, while a cutaneous manifestation may be limited. Furthermore, because bone produces the highest tissue resistance to electricity, it consequently experiences the most heat, thus potentially setting up the perfect conditions for an overlying compartment syndrome21. Chemical burns often have a progressive effect due to infiltration into deeper tissue; therefore, they should be considered as a deep partial-thickness or full-thickness burn until proven otherwise25. Burn depth was originally identified and classified by Par´e26 into first, second, third, and fourth-degree burns (Fig. 1, A, B). Initial Assessment and Management of Burn Patients with Orthopaedic Injuries Initial care of burn patients includes adherence to the Advanced Trauma Life Support (ATLS) protocol that was established by the American College of
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Fig. 3 Fig. 3A Diagram showing the total body surface area (TBSA) percentage in the rule-of-nines calculation. To note the presence of inhalation injuries, increase the percentage of TBSA by 20%120. Fig. 3B Diagram showing TBSA percentage in the LundBrowder chart calculation. Fig. 3C Fluid resuscitation formulas utilized for the initial management following burn injury are shown. The Parkland and modified Brooke formulas are both widely utilized by burn units. The main difference between the two involves the acute use of colloid fluid in the Brooke formula. These formulas are applicable up to twenty-four hours after acute burn injury, after which colloid-based fluids are mostly utilized. For example, according to the Parkland formula, fluid resuscitation for a man weighing 80 kg whose burns involve 40% of the TBSA would amount to 12,800 mL for the first twenty-four hours.
Surgeons27. Although burns are visually disturbing and cause substantial pain, the treating team should not become distracted by the burn and instead should focus on completing the ATLS milestones, including attention to the ABCs (airway, breathing, and circulation)7. In addition, there are specific aspects of the burn that should be addressed during the initial evaluation, both to adequately manage the patient and to identify the need for transferring the patient to a burn center (Tables I and II). Resuscitation and Fluid Replacement Fluid resuscitation is the cornerstone of acute management and should precede initial wound care28. Establishing intravenous access is attained with peripheral catheters or through central access when
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superficial veins are injured or thrombosed. Foley catheterization is imperative to accurately track urine output. Because burn edema contains isotonic fluid29, an isotonic crystalloid solution such as normal saline solution or lactated Ringer’s solution is utilized for acute resuscitation21. To calculate fluid requirements, the percent total body surface area must be determined with use of the rule of nines (a method in which the body is divided into sections of 9% or multiples of 9% to aid in the estimation of the extent of adult body surface that has been burned) or the LundBrowder chart (a method for classifying the extent of body surface that has been burned in children)30 (Fig. 3, A, B). The rate of fluid administration for the first twenty-four hours can then be calculated
with use of the traditional Parkland formula31 or modified Brooke formula32 (Fig. 3, C), which have been shown to produce similar clinical outcomes33. These formulas are only starting points in resuscitation, and fluid rates must be modified according to urine output, heart rate, base deficits, and lactate levels34. The minimum recommended urine output is 0.5 to 1.0 mL/kg per hour or 30 to 50 mL of urine per hour in adults and 1 to 2 mL/kg per hour in children, while a pulse rate ,110 beats per minute is generally considered to reflect adequate volume resuscitation21. Wound Assessment Following stabilization, burn wounds can be cleaned with soap and water in order to
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Criteria for Referral of Patient to a Burn Center*
1. Partial-thickness burns affecting .10% of total body surface area 2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints 3. Third-degree burns in any age group 4. Electrical burns, including lightning injury 5. Chemical burns 6. Inhalation injury 7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality 8. Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols. 9. Burned children in hospitals that do not have qualified personnel or equipment for the care of children 10. Burn injury in patients who will require special social, emotional, or rehabilitative intervention *The information contained in this table is in accordance with the published Guidelines for the Operation of Burn Centers (p 79-86), Resources for Optimal Care of the Injured Patient 2006, Committee on Trauma, American College of Surgeons.
clear the remaining debris and so that a formal evaluation of burn degree and size can be performed. The relationship of burns to underlying joints or fractures should be carefully recorded, and a high index of suspicion should be maintained for the possibility of an open fracture or traumatic arthrotomy. Unfortunately, the literature currently provides no accepted definition about which burn grade corresponds to a so-called “open injury” when the burn is located over a fracture or joint. In spite of this, it is the opinion of the authors that third or fourth-degree burns are deep enough to place the underlying fracture or joint at risk for infection; therefore, strong consideration should be given to the performance of operative irrigation and debridement with subsequent consultation for soft-tissue coverage. Compartment syndrome can occur in association with burns and is similar but different from compartment syndrome resulting from other traumatic causes. Normal skin itself is rarely the cause of constriction and elevated compartment pressure because skin is acutely elastic. It is the inelastic fascia covering the muscle that causes increased pressure and needs to be released. However, burned skin immediately loses its elasticity, and subsequent scarring actually contracts the skin, thus increasing compartment pressures. Pain on
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passive stretch is not as reliable a clinical sign of compartment syndrome in burns as in other trauma because the burn may render the limb hypersensitive to any physical stimulus or, conversely, be so extensive as to render the limb insensate. Therefore, a high degree of suspicion and a low threshold for measuring pressure and performing releasing incisions is appropriate. Compartment syndrome is especially likely in the setting of highenergy fractures with burns, circumferential burn wounds, and electrical burns5,6,11 due to the development of inelastic eschar, which acts like a tourniquet on the extremity3. Therefore, cutaneous eschars, which do not blanch with pressure and are insensate, should be evaluated regularly and treated with either escharotomy or fasciotomy when analgesic requirements or compartment pressures increase. Prevention of Infection All burn wounds should be covered to minimize fluid loss and heat loss. A variety of techniques have been successfully used, including coverage with a plastic wrap or with a standard dressing of gauze impregnated with saline solution or soft paraffin to minimize evaporative heat loss. Topical agents with antiseptic properties should be routinely used for all burn wounds in the acute period35-37. Silver sulfadiazine
(Silvadene) is the most commonly utilized agent for first and second-degree burns and some third-degree burns due to its efficient cutaneous penetration and broad antibacterial spectrum37. Acticoat (Smith & Nephew), a gauze material impregnated with a silver compound, also has excellent antibacterial activity against methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE)38,39. Mafenide acetate can be utilized on third-degree or fourthdegree burns due to its ability to penetrate through eschar and prevent deep infection40,41. Burns that develop pseudomonas infections are treated with sulfamylon cream (mafenide acetate cream). Burn wounds that involve open fractures are usually left open for serial debridement or until definitive coverage or closure can be performed3. For these wounds, negative-pressure dressings, including vacuum-assisted closure with open-pore foam, are recommended21. Intermittent suction is preferred as it favors the formation of granulation tissue42. The use of universal systemic antibiotics in burn patients does not have strong support in the literature, leading to a recommendation against routine use43. Systemic antibiotic prophylaxis is mandated in burn patients only when open fractures or traumatic arthrotomies are
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present. Total-thickness burns over a joint are often treated in the same manner as an open fracture or arthrotomy. Similar to the coverage that they provide in the treatment of non-burn patients, initial antibiotics should provide good coverage against Staphylococci and aerobic gramnegative bacilli and should be initiated within six hours after injury44-46. Pain Management Attaining adequate analgesia in burn patients can be challenging and may require anesthesia consultation47,48. Altered basal metabolism and splanchnic vessel perfusion can affect hepatic function and potentially change the predicted duration of effect of analgesics such as opioids and acetaminophen. Short-acting narcotics taken orally or applied transdermally are generally well tolerated49, as are anxiolytic medications50. Indwelling epidural catheters, although effective for analgesia51, should not be utilized regularly because they may mask symptoms of compartment syndrome. Management of Acute Fractures Nonoperative Treatment Nonoperative management has been the historical preference for the treatment of most fractures associated with burns. In 1943, Bodenham11 recommended postponing manipulation of any fractured limb with an ipsilateral burn injury until the burn wound had been definitively treated. Similar recommendations were made by several authors throughout the Second World War and beyond8,10,47,52, with splint and traction being the preferred methods of treatment. General restoration of length and alignment is appropriate, but aggressive attempts at closed reduction are not warranted. Due to a lack of comparative studies, the current indications for nonoperative management of fractures in burn patients are based on expert opinion. Initial nonoperative treatment is the only available option for patients who are considered medically unfit for surgery. Nonoperative management is appropriate for any minimally displaced fracture in which alignment can be maintained with use of a
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well-padded splint. Due to the increased risk of compartment syndrome and the inability to sequentially assess the skin, circumferential casting is not recommended in patients who are unconscious53 or have severe burns. If the burn wound is included within the splint, regular wound surveillance and dressing changes should be performed through a cast window. Placement of external fixators in the intensive care unit is one option for these patients. Operative Treatment Investigations in the latter half of the twentieth century determined that open reduction and internal fixation of articular or comminuted fractures could be performed safely in burn patients. In 1962, Teplitz demonstrated that most burn wounds remained sterile for up to forty-eight hours after injury54. In an experimental study in dogs, Fitts et al. reported no increased infection rates for long-bone fractures with an overlying third-degree burn treated with open reduction and intramedullary nailing versus plaster casting48. Using the same model, Grisolia and colleagues55,56 found a higher union rate of fractures treated immediately with intramedullary nailing as compared with the rate in fractures treated after forty-eight hours41,42. They concluded that operative intervention did not increase the risk of infection and instead was likely to be preventative of infection because it protected against further soft-tissue injury and permitted healing. Following these successful experiments, early internal fixation was attempted in several clinical studies, with good results, although these studies were uncontrolled retrospective case series. Saffle and colleagues reported successful union and wound-healing following early internal fixation of fractures in a small series of nine burn patients, only three of whom had burns directly over the fracture site5. Other authors also reported positive results but suggested that internal fixation should be acutely attempted only within twenty-four to forty-eight hours following injury, with external fixation indicated thereafter4,12,50,57. The largest cohort of
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burn patients undergoing early operative management was reported by Dossett and colleagues6. They found that early internal fracture fixation, performed within forty-eight hours after injury (and when adequate fluid resuscitation and treatment of other injuries had already been performed), was safest in comparison with delayed fixation or inadequate resuscitation. The authors reported that there were no wound infections in any of the orthopaedic surgical incisions of the 101 patients that they reviewed. Rosenkranz and Sheridan reported similar success in a series of fifty-three patients49. It should be noted that no prospective observational or randomized controlled trials have been conducted with regard to the operative treatment of orthopaedic injuries in burn patients; therefore, no high-quality recommendations can be made regarding the placement of surgical incisions or the choice between the use of internal versus external fixation. Nevertheless, the above studies point to internal fracture fixation as being a relatively safe procedure in adequately resuscitated burn patients, provided that the fixation is performed within forty-eight hours after injury. Although it is preferable to place surgical incisions outside of deeply burnt tissue, attaining proper exposure facilitates fracture reduction, thus accelerating the healing of soft tissue and ultimately allowing faster mobilization of the patient49. External fixation remains an excellent choice in a damagecontrol situation when dealing with extensive soft-tissue loss, a grossly contaminated wound, or when internal fixation cannot be achieved within fortyeight hours after injury. In cases of severe fourth-degree burns and complex fractures, amputation may give superior results to limb salvage. Also, amputation may reduce the systemic physiological burden to the patient and enhance the chances of survival. The decision to proceed with either amputation or reconstruction is based primarily on the extent of soft-tissue injury and the feasibility of both recovery and coverage58.
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Fig. 4 Fig. 4A Clinical photograph of the leg of a patient with third-degree burns to the left leg and dorsum of the foot. Fig. 4B Wound coverage was achieved with a porcine xenograft, which was applied under sterile conditions to the debrided base of the burn wound. The artificial dermis serves to prevent infection, prevent fluid loss, and prevent surrounding skin contraction. The wound healed adequately.
On the basis of their experience with wounds resulting from open fractures, the authors recommend that fracture wound closure should always be attempted at the initial operation unless tension-free closure is not possible or heavy bacterial contamination is present. If left open, such wounds should be subsequently cared for with serial debridements every forty-eight to seventytwo hours, followed by definitive closure within seven days after injury59,60. Definitive closure may be achieved by direct skin apposition or grafting techniques. Split-thickness allograft or xenograft (Fig. 4) represents the most widely utilized form of biological wound coverage for burns and functions to decrease fluid loss, facilitate dressing change, and diminish local bacterial growth. The potential for allograft rejection seven to fourteen days after implantation due to inflammatory cell infiltrate has led to interest in developing artificial dermal replacements. Artificial dermis products have been shown to prevent infection,
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decrease fluid loss, and provide cosmetically acceptable results61-63. However, their high cost and unpredictable rate of rejection21,64 preclude their regular use when extensive coverage is required. Management of Complications The development of complications in burned patients with associated orthopaedic injuries depends on the mechanism of thermal injury, the depth (grade) and extent (percent of total body surface area) of the burn, the proximity of joints to the burn, and on whether associated fractures were open or heavily contaminated. Orthopaedic complications that must be managed include joint contractures, heterotopic ossification, osteomyelitis, malunion, and nonunion. Other complications include weakness and cosmetic deformity. Joint Contractures According to the results of studies of a total of 3045 patients, between 5% and 40% of patients with burn injuries will
develop joint contractures65-69. In these patients, thermal and electrical burns caused 36.7% (thirty-three of ninety) and 13.3% (twelve of ninety) of the contractures, respectively, with the upper limbs more often involved69-71. Joint contractures arise through replacement of damaged skin with pathological scar tissue of insufficient extensibility and length, resulting in loss of joint motion70. Burn patients are at particular risk for developing contractures due to prolonged immobilization, limited motion as a result of pain, and loss of function as a result of soft-tissue injury69. Specific risk factors for the development of contractures include longer hospital stay, younger patient age, full-thickness burns, burns to the neck and/or upper extremities, multiple surgical procedures, and burns that cross a major joint67,69. A preventative approach that addresses these reasons and facilitates early passive and active range of motion represents the optimal prevention and initial treatment for contractures72.
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TABLE III
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Grades of Recommendation121 for Acute and Chronic Management of Burn Patients with Associated Orthopaedic Injuries Grade*
Acute fluid resuscitation of all burn patients with crystalloid solution following either the Parkland or modified Brooke formulas
B
Initiate degree-appropriate dressing, topical care and/or vacuum-assisted closure in acute and sub-acute burn care
B
Systemic antibiotic prophylaxis only for burn patients with presence of open fractures or traumatic arthrotomy
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May incorporate burn into surgical incision if (1) wound is not grossly contaminated and (2) surgery is performed ,48 hr after burn injury
C
Early internal fixation within 48 hr after injury if patient is stable and the wound is not grossly contaminated
B
Acute closure of open wound if (1) wound is not under tension and (2) there is no gross contamination
C
Split-thickness skin-grafting for second and third-degree burns
B
Routine use of static or dynamic splinting in early postoperative period to prevent contractures
I
Routine use of heterotopic ossification prophylaxis in burn patients
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*Grade A indicates good evidence (Level-I studies with consistent findings) for or against recommending intervention. Grade B, fair evidence (Level-II or III studies with consistent findings) for or against recommending intervention. Grade C, conflicting or poor-quality evidence (Level-IV or V studies) not allowing a recommendation for or against intervention. Grade I, there is insufficient evidence to make a recommendation.
Making a recommendation with regard to the regular use of splinting for acute contracture prevention in burn patients is difficult because of the paucity of studies on this subject. However, dynamic splinting is a reasonable firstline therapy for any decreased range of motion that is observed or anticipated in the subacute and chronic period. Dynamic splinting involves applying a mechanical load in the opposite direction of the contractile force within a wound to theoretically reduce wound or scar contraction73,74. Dynamic splint application should be delayed until a decrease in joint motion is noted, although static splinting in alternating extremes of arc of motion may be beneficial to prophylactically prevent contracture74. To our knowledge as of the time of this writing, there are currently only case reports describing the ideal application time or duration of application for static splints, and therefore their regular use in the acute period cannot be recommended strongly66. The use of dynamic splinting in the subacute and chronic period is supported for posttraumatic stiffness75-77. Huang and
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colleagues, reporting on 625 burn patients, found that dynamic splinting dramatically reduced the incidence of joint contracture; only 7.3% of patients who wore the splints for six months had contracture, as compared with 55% of patients who wore the splint for less than six months and 62% of patients who did not wear the splint at all78. Furthermore, Richard and colleagues reported improved elbow range of motion with dynamic splinting versus static splinting in a case report of a patient with bilateral burn-related elbow contractures79. In consideration of these limited but positive findings, the use of dynamic splinting for the treatment of joint contracture appears to be a reasonable first-line therapy when contracture is noted in the subacute and chronic period. Proper splint fitting is essential and should be checked regularly due to fluctuations in limb swelling80. If minimal improvement is noted with use of dynamic splinting, then the early use of plastic surgery for scar excision as well as the use of skin grafts, local and distant flaps, and tissue expanders combined with dynamic
splinting has been reported as being an effective secondary measure for improving the range of motion73,81-84. Simple surgical or z-plasty release of scar tissue may also be considered and should be performed in line with the axis of joint rotation85. Heterotopic Ossification Johnson provided the first description of heterotopic ossification in burn patients in 195786. Heterotopic ossification refers to the formation of bone in nonosseous tissue in response to longstanding soft-tissue inflammation87,88. Heterotopic ossification has occurred in 1% to 3% of 5812 burn patients89-93and has been associated with the presence of full-thickness burns94, prolonged immobilization, forceful passive physical therapy, and the presence of infection95-97. Heterotopic ossification occurs across major joints and muscle groups98-101, with the elbow, shoulder, and hip representing the most commonly described sites81,85,86. Interestingly, the site of heterotopic ossification formation is not necessarily identical to the site of burned tissue and perhaps represents a
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Fig. 5 Acute treatment algorithm for burn patients with associated orthopaedic injuries, based on the current available literature (Level-III to Level-V evidence studies). ORIF = open reduction and internal fixation, and VAC = vacuum-assisted closure.
sequela of the systemic inflammatory response to burns91. Suspicion for heterotopic ossification should arise in the context of decreased range of motion, which can occur as early as three weeks after injury89. Radiography, bone scan93, and
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ultrasonography are effective modalities for the early diagnosis of heterotopic ossification102. Once the diagnosis of heterotopic ossification is made, restricted passive and active-assisted motion of the affected joints should be commenced98,103-106 followed by
consideration to begin medical therapy and/or manipulation under anesthesia107. If surgical resection is contemplated, then advanced imaging studies (MRI or CT) should be performed to identify the relationship to nearby neurovascular structures, which often
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penetrate through heterotopic ossification108-110. Surgical resection should be considered if conservative measures fail108. Recurrence after surgical resection is common, but recurrence rates are lower if the heterotopic ossification is “mature” rather than “active” at the time of resection111-116. Resection of heterotopic ossification should therefore be delayed until radiographic maturation is observed, and maturation commonly occurs twelve to twenty-four months after the injury111-116. On the other hand, some authors recommend that, to achieve postoperative functional range of motion, surgery should not be delayed for more than twelve months117. Another method to minimize the recurrence rate is to utilize radiation or oral medication to prevent the formation of heterotopic ossification in the postoperative period. The use of radiation therapy or indomethacin has been suggested for the prevention of heterotopic ossification in patients following total hip arthroplasty or fracture fixation; little data exist with regard to burn patients, however, which precludes these therapies from being routinely recommended, particularly for patients with acute fracture118-120. Malunion and Nonunion The complications of malunion and nonunion are seen with increased frequency in fractures associated with burns. However, only limited literature exists regarding the unique features of malunion and nonunion in burn patients. Case reports describing the occurrence of malunion highlight the increased risk of infection after revision fixation and suggest that the increased risk is due to the poor quality of overlying soft tissue57,121. Careful preoperative planning, plastic surgery consultation for skin coverage, and vigilant postoperative monitoring for infection should be considered when burn patients are being treated for malunion or nonunion. The average healing time for fractures associated with burns is unknown but is probably increased compared with that for fractures that are not associated with burns, and therefore delayed
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unions are common. The percentage of fractures that progress to nonunion in burn patients is also presumably greater than that in non-burn patients, but this theory has not been clearly validated in the literature. The scarred soft-tissue envelope and the potential for poor blood supply to the fracture site complicate the treatment of nonunion. Summary A systematic approach (Fig. 5) that prioritizes ATLS evaluation, fluid resuscitation, and multidisciplinary involvement is essential for optimizing the outcome of burn patients who have orthopaedic injuries. In addition, it is important to look for any associated smoke inhalation or carbon monoxide poisoning and to document the extent (i.e., the percent of total body surface area) and depth (grade) of the burn. The acute orthopaedic evaluation should focus on the identification and treatment of limb-threatening conditions such as fractures (open and closed), dislocations, circumferential eschars, compartment syndrome, and limb hypoperfusion. Historically, fracture stabilization by external fixation has been considered to be the safest method of treatment. However, definitive internal fixation within the first forty-eight hours after injury is associated with improved osseous healing and infection rates in selected patients, but such advantages must be balanced against the risk of hemodynamic instability and a generalized hypermetabolic state. The lack of Level-I and Level-II studies on this topic in the current literature limits the strength of recommendations for interventions in the acute period (Table III) and points out the need for prospective studies in the future. Source of Funding There were no sources of funding for this study. Saad M. AlQahtani, MD, MSc(C)1, Mohammad M. Alzahrani, MD, MSc(C)1, Alberto Carli, MD, MSc1, Edward J. Harvey, MD, MSc, FRCSC1
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1Division
of Orthopaedic Surgery, McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, Room B5.159.5, Montreal, Quebec, Canada H3G 1A4 E-mail address for E.J. Harvey:
[email protected]
References 1. Grout P, Horsley M, Touquet R. Epidemiology of burns presenting to an accident and emergency department. Arch Emerg Med. 1993 Jun;10(2):100-7. 2. Micheels J, Lamy M, Jacquemin D. [Role of a surgical emergency department in the management of a disaster bringing a great number of patients with burns] [French]. Acta Chir Belg. 1986 May-Jun;86(3):192-6. 3. Pruitt BA Jr. Management of burns in the multiple injury patient. Surg Clin North Am. 1970 Dec;50(6):1283-300. 4. Purdue GF, Hunt JL. Multiple trauma and the burn patient. Am J Surg. 1989 Dec;158(6):536-9. 5. Saffle JR, Schnelby A, Hofmann A, Warden GD. The management of fractures in thermally injured patients. J Trauma. 1983 Oct;23(10): 902-10. 6. Dossett AB, Hunt JL, Purdue GF, Schlegel JD. Early orthopedic intervention in burn patients with major fractures. J Trauma. 1991 Jul;31(7): 888-92; discussion 892-3. 7. Frye KE, Luterman A. Burns and fractures. Orthop Nurs. 1999 Jan-Feb;18(1):30-5. 8. Dowling JA, Omer GE, Moncrief JA. Treatment of fractures in burn patients. J Trauma. 1968 May;8(3):465-74. 9. Evans EB, Smith JR. Bone and joint changes following burns; a roentgenographic study; preliminary report. J Bone Joint Surg Am. 1959 Jul;41(5):785-99. 10. Urist MR, Quigley TB. Use of skeletal traction for mass treatment of compound fractures; a summary of experiences with 4,290 cases during World War II.AMA Arch Surg. 1951 Dec; 63(6):834-44. 11. Bodenham DC. The problem of fractures with associated burn injuries: principles of treatment. Proc R Soc Med. 1943;36:657-62. 12. Wong L, Grande CM, Munster AM. Burns and associated nonthermal trauma: an analysis of management, outcome, and relation to the Injury Severity Score. J Burn Care Rehabil. 1989 Nov-Dec;10(6):512-6. 13. Institute for Health Metrics and Evaluation. The global burden of disease: 2010 update. 2012; viz.healthmetricsandevaluation.org/ gbd-compare/. Accessed 2013 Dec 1.
14. Murray C, Lopez A. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. World Health Organization. 2006. http:// whqlibdoc.who.int/publications/1996/ 0965546608_eng.pdf. Accessed 2014 May 14. 15. Harms BA, Bodai BI, Smith M, Gunther R, Flynn J, Demling RH. Prostaglandin release and altered microvascular integrity after burn injury. J Surg Res. 1981 Oct;31(4):274-80. 16. Aulick LH, Wilmore DW, Mason AD Jr, Pruitt BA Jr. Influence of the burn wound on
11
|
B u r n M a n a g e m e n t i n O r t h o p a e d i c Tr a u m a
peripheral circulation in thermally injured patients. Am J Physiol. 1977 Oct;233(4):H520-6.
17. Jackson DM. [The diagnosis of the depth of burning].Br J Surg. 1953 May;40(164):588-96.
38. Yin HQ, Langford R, Burrell RE. Comparative
18. Martyn J, Wilson RS, Burke JF. Right
evaluation of the antimicrobial activity of ACTICOAT antimicrobial barrier dressing. J Burn Care Rehabil. 1999 May-Jun;20(3):195-200.
ventricular function and pulmonary hemodynamics during dopamine infusion in burned patients. Chest. 1986 Mar;89(3):357-60.
19. Crum RL, Dominic W, Hansbrough JF, Shackford SR, Brown MR. Cardiovascular and neurohumoral responses following burn injury. Arch Surg. 1990 Aug;125(8):1065-9. ¨ 20. Holm C, Horbrand F, von Donnersmarck GH, ¨ Muhlbauer W. Acute renal failure in severely burned patients. Burns. 1999 Mar;25(2):171-8.
21. Steinstraesser L, Al-Benna S. Acute management of burn/electrical injuries. In: Neligan PC, editor. Plastic surgery. 3rd ed, Vol 4. New York: Saunders; 2013:393-434.
22. Kramer GC. Pathophysiology of burn shock and burn edema. In: Herndon DN, ed. Total burn care. 4th. ed. London: Saunders; 2012:103-13.
23. Hobbs CJ. When are burns not accidental? Arch Dis Child. 1986 Apr;61(4):357-61.
24. Ding YL, Pu SS, Pan ZL, Lu X, Miao SG, Han CM, Wang F. Extensive scalds following accidental immersion in hot water pools. Burns Incl Therm Inj. 1987 Aug;13(4):305-8.
25. Kao DS, Hijjawi J. Cold and chemical injury to the upper extremity. In: Neligan PC, ed. Plastic Surgery. 3rd ed, Vol 4. New York: Saunders; 2013:456-67.
26. Pare´ A. (1510-1590). In: Thomas J, translator. The works of that famous chirurgion Ambrose Parey translated out of Latine and compared with the French. London: Th. Cotes and R. Young; 1634. 27. American College of Surgeons. Advanced trauma life support. 2014. http://www.facs.org/ trauma/atls/. Accessed 2014 Jan 10.
28. Kauvar DS, Wolf SE, Wade CE, Cancio LC, Renz EM, Holcomb JB. Burns sustained in combat explosions in Operations Iraqi and Enduring Freedom (OIF/OEF explosion burns). Burns. 2006 Nov;32(7):853-7. Epub 2006 Aug 8.
29. Baxter CR. Fluid volume and electrolyte changes of the early postburn period. Clin Plast Surg. 1974 Oct;1(4):693-703.
30. Lund C, Browder N. The estimation of areas of burns. Surg Gynecol Obstet. 1944;79:352-8.
31. Baxter CR, Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci. 1968 Aug 14;150(3):874-94.
32. Pruitt BA Jr. Fluid and electrolyte replacement in the burned patient. Surg Clin North Am. 1978 Dec;58(6):1291-312.
33. Cancio LC, Cha´ vez S, Alvarado-Ortega M, Barillo DJ, Walker SC, McManus AT, Goodwin CW. Predicting increased fluid requirements during the resuscitation of thermally injured patients. J Trauma. 2004 Feb;56(2):404-13, discussion:413-4. 34. Purdue GF, Arnoldo BD, Hunt JL. Acute assessment and management of burn injuries. Phys Med Rehabil Clin N Am. 2011 May;22(2): 201-12, v.
35. McManus WF, Goodwin CW, Mason AD Jr, Pruitt BA Jr. Burn wound infection. J Trauma. 1981 Sep;21(9):753-6.
36. Monafo WW, West MA. Current treatment recommendations for topical burn therapy. Drugs. 1990 Sep;40(3):364-73.
12
37. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2006 Apr;19(2):403-34.
39. Heggers J, Goodheart RE, Washington J, McCoy L, Carino E, Dang T, Edgar P, Maness C, Chinkes D. Therapeutic efficacy of three silver dressings in an infected animal model. J Burn Care Rehabil. 2005 Jan-Feb;26(1):53-6.
grafts and Etheron prosthetic sponge. J Trauma. 1964 Sep;4:682-6.
57. Curtis MJ, Clarke JA. Skeletal injury in thermal trauma: a review of management. Injury. 1989 Nov;20(6):333-6. 58. MacKenzie EJ, Bosse MJ, Kellam JF, Burgess AR, Webb LX, Swiontkowski MF, Sanders R, Jones AL, McAndrew MP, Patterson B, McCarthy ML, Rohde CA; LEAP Study Group. Factors influencing the decision to amputate or reconstruct after high-energy lower extremity trauma. J Trauma. 2002 Apr;52(4):641-9.
40. Brown TPLH, Cancio LC, McManus AT, Mason AD Jr. Survival benefit conferred by topical antimicrobial preparations in burn patients: a historical perspective. J Trauma. 2004 Apr;56(4):863-6.
59. Hohmann E, Tetsworth K, Radziejowski MJ,
41. Stefanides MM Sr, Copeland CE, Kominos SD, Yee RB. In vitro penetration of topical antiseptics through eschar of burn patients. Ann Surg. 1976 Apr;183(4):358-64.
60. Russell GG, Henderson R, Arnett G. Primary or delayed closure for open tibial fractures. J Bone Joint Surg Br. 1990 Jan;72(1):125-8.
42. Streubel PN, Stinner DJ, Obremskey WT. Use of negative-pressure wound therapy in orthopaedic trauma. J Am Acad Orthop Surg. 2012 Sep;20(9):564-74.
43. Avni T, Levcovich A, Ad-El DD, Leibovici L, Paul M. Prophylactic antibiotics for burns patients: systematic review and meta-analysis. BMJ. 2010;340:c241. Epub 2010 Feb 15. 44. Patzakis MJ, Wilkins J, Moore TM. Considerations in reducing the infection rate in open tibial fractures. Clin Orthop Relat Res. 1983 Sep;(178):36-41. 45. Seligson D, Henry SL. Treatment of compound fractures. Am J Surg. 1991 Jun;161(6):693-701. 46. Patzakis MJ, Bains RS, Lee J, Shepherd L, Singer G, Ressler R, Harvey F, Holtom P. Prospective, randomized, double-blind study comparing single-agent antibiotic therapy, ciprofloxacin, to combination antibiotic therapy in open fracture wounds. J Orthop Trauma. 2000 Nov;14(8):529-33. 47. Warthen HJ. The Treatment of Burns Complicated by Fractures of the Extremities. Ann Surg. 1944 Apr;119(4):526-31. 48. Fitts WT Jr, Roberts B, Grippe WJ, Muir MW, Allam MW. The treatment of fractures complicated by contiguous burns; an experimental study in dogs. Surg Gynecol Obstet. 1953 Nov;97(5):551-64. 49. Rosenkranz KM, Sheridan R. Management of the burned trauma patient: balancing conflicting priorities. Burns. 2002 Nov;28(7):665-9. 50. Purdue GF, Hunt JL, Layton TR, Copeland CE, delMundo AG, Baxter CR. Burns in motor vehicle accidents. J Trauma. 1985 Mar;25(3):216-9. 51. Novak J, Papp T, Zaborszky A. Burns associated with mechanical injuries. Burns. 1977;4:197-206.
52. Evans EB. Orthopaedic measures in the treatment of severe burns. J Bone Joint Surg Am. 1966 Jun;48(4):643-69. 53. Drager J, Carli A, Matache BA, Berry GK, Reindl R, Harvey EJ. Circumferential Casting of Distal Radius Fractures. J Orthop Trauma. 2013 Dec 30. [Epub ahead of print]. 54. Teplitz C. The burn autopsy. US Surg Res Unit Res Rep.1962;228:41. 55. Grisolia A, Forrest WJ, Peltier LF. The treatment of fractures complicated by burns: an experimental study. J Trauma. 1963 May;3:259-67. 56. Grisolia A, Peltier LF. The treatment of fractures complicated by burns. The use of skin
Wiesniewski TF. Comparison of delayed and primary wound closure in the treatment of open tibial fractures. Arch Orthop Trauma Surg. 2007 Feb;127(2):131-6. Epub 2006 Aug 31.
¨ 61. Lagus H, Sarlomo-Rikala M, Bohling T, Vuola J. Prospective study on burns treated with Integra®, acellulose sponge and split thickness skin graft: comparative clinical and histological study—randomized controlled trial. Burns. 2013 Dec;39(8):1577-87. Epub 2013 Jul 20.
62. Heimbach D, Luterman A, Burke J, Cram A, Herndon D, Hunt J, Jordan M, McManus W, Solem L, Warden G, et al. Artificial dermis for major burns. A multi-center randomized clinical trial. Ann Surg. 1988 Sep;208(3): 313-20. 63. Shevchenko R, Sibbons P, Sharpe J, James SE. A novel skin substitute biomaterial to treat full-thickness wounds in a burns emergency care. In: Mikhalovsky S. Biodefence: advanced materials and methods for health protection. Springer; 2011:247-55. 64. Atiyeh BS, Hayek SN, Gunn SW. New technologies for burn wound closure and healing—review of the literature. Burns. 2005 Dec;31(8):944-56. Epub 2005 Nov 4. 65. Dobbs ER, Curreri PW. Burns: analysis of results of physical therapy in 681 patients. J Trauma. 1972 Mar;12(3):242-8. 66. Esselman PC, Thombs BD, Magyar-Russell G, Fauerbach JA. Burn rehabilitation: state of the science. Am J Phys Med Rehabil. 2006 Apr;85(4): 383-413. 67. Gangemi EN, Gregori D, Berchialla P, Zingarelli E, Cairo M, Bollero D, Ganem J, Capocelli R, Cuccuru F, Cassano P, Risso D, Stella M. Epidemiology and risk factors for pathologic scarring after burn wounds. Arch Facial Plast Surg. 2008 Mar-Apr;10(2):93-102. 68. Kraemer MD, Jones T, Deitch EA. Burn contractures: incidence, predisposing factors, and results of surgical therapy. J Burn Care Rehabil. 1988 May-Jun;9(3):261-5. 69. Schneider JC, Holavanahalli R, Helm P, Goldstein R, Kowalske K. Contractures in burn injury: defining the problem. J Burn Care Res. 2006 Jul-Aug;27(4):508-14. 70. Puri V, Khare N, Venkateshwaran N, Bharadwaj S, Choudhary S, Deshpande O, Borkar R. Serial splintage: Preoperative treatment of upper limb contracture. Burns. 2013 Sep;39(6):1096-100. Epub 2013 Feb 28. 71. Schneider JC, Holavanahalli R, Helm P, O’Neil C, Goldstein R, Kowalske K. Contractures in burn injury part II: investigating joints of the hand. J Burn Care Res. 2008 Jul-Aug;29(4): 606-13.
OCTOBER 2014
· VOLUME 2, ISSUE 10 · e4
B u r n M a n a g e m e n t i n O r t h o p a e d i c Tr a u m a
72. Schwarz RJ. Management of postburn contractures of the upper extremity. J Burn Care Res. 2007 Mar-Apr;28(2):212-9.
73. Harrison CA, MacNeil S. The mechanism of
89. Richards AM, Klaassen MF. Heterotopic ossification after severe burns: a report of three cases and review of the literature. Burns. 1997 Feb;23(1):64-8.
skin graft contraction: an update on current research and potential future therapies. Burns. 2008 Mar;34(2):153-63. Epub 2008 Jan 15.
90. Kolar J, Vrabec R. Periarticular soft-tissue changes as a late consequence of burns. J Bone Joint Surg Am. 1959 Jan;41-A(1):103-11.
74. Schouten HJ, Nieuwenhuis MK, van Zuijlen
91. Evans EB. Heterotopic bone formation in thermal burns. Clin Orthop Relat Res. 1991 Feb; (263):94-101.
PP. A review on static splinting therapy to prevent burn scar contracture: do clinical and experimental data warrant its clinical application? Burns. 2012 Feb;38(1):19-25. Epub 2011 Aug 9.
75. Shewring DJ, Beaudet M, Carvell JE. Reversed dynamic slings: results of use in the treatment of post-traumatic flexion contractures of the elbow. Injury. 1991 Sep; 22(5):400-2.
76. Gelinas JJ, Faber KJ, Patterson SD, King GJ. The effectiveness of turnbuckle splinting for elbow contractures. J Bone Joint Surg Br. 2000 Jan;82(1):74-8.
77. Lindenhovius AL, Doornberg JN, Brouwer KM, Jupiter JB, Mudgal CS, Ring D. A prospective randomized controlled trial of dynamic versus static progressive elbow splinting for posttraumatic elbow stiffness. J Bone Joint Surg Am. 2012 Apr 18;94(8):694-700.
78. Huang TT, Blackwell SJ, Lewis SR. Ten years of experience in managing patients with burn contractures of axilla, elbow, wrist, and knee joints. Plast Reconstr Surg. 1978 Jan;61(1):70-6.
79. Richard R, Baryza MJ, Carr JA, Dewey WS,
92. Elledge ES, Smith AA, McManus WF, Pruitt BA Jr. Heterotopic bone formation in burned patients. J Trauma. 1988 May;28(5):684-7. 93. Gaur A, Sinclair M, Caruso E, Peretti G, Zaleske D. Heterotopic ossification around the elbow following burns in children: results after excision. J Bone Joint Surg Am. 2003 Aug; 85(8):1538-43. 94. Jay MS, Saphyakhajon P, Scott R, Linder CW, Grossman BJ. Bone and joint changes following burn injury. Clin Pediatr (Phila). 1981 Nov;20 (11):734-6. 95. Nassabi H, Raff T, Germann G. Manifestation of multifocal heterotopic ossifications with unusual locations as a complication after severe burn injury. Burns. 1996 Sep;22(6):500-3. 96. Klein MB, Logsetty S, Costa B, Deters L, Rue TC, Carrougher GJ, Pickens M, Engrav LH. Extended time to wound closure is associated with increased risk of heterotopic ossification of the elbow. J Burn Care Res. 2007 May-Jun; 28(3):447-50.
Dougherty ME, Forbes-Duchart L, Franzen BJ, Healey T, Lester ME, Li SK, Moore M, Nakamura D, Nedelec B, Niszczak J, Parry IS, Quick CD, Serghiou M, Ward RS, Ware L, Young A. Burn rehabilitation and research: proceedings of a consensus summit. J Burn Care Res. 2009 JulAug;30(4):543-73.
97. Zaman SR. Heterotopic ossification of the elbows in a major petrol burn. BMJ Case Rep. 2012 Aug 27; 2012.
80. Gordon MD, Gottschlich MM, Helvig EI,
99. Orzel JA, Rudd TG. Heterotopic bone formation: clinical, laboratory, and imaging correlation. J Nucl Med. 1985 Feb;26(2): 125-32.
Marvin JA, Richard RL. Review of evidencedbased practice for the prevention of pressure sores in burn patients. J Burn Care Rehabil. 2004 Sep-Oct;25(5):388-410.
81. Karacaoglan N, Uysal A. Reconstruction of postburn scar contracture of the neck by expanded skin flaps. Burns. 1994 Dec;20(6): 547-50.
82. Mingli Z, Dawei W, Lan H. The application of skin external expander to postburn advanced scar contracture. Plast Reconstr Surg. 1995 Dec; 96(7):1600-7. ˘ 83. Karacaoglan N, Uysal A. Use of seven-flap plasty for the treatment of axillary and groin postburn contractures. Burns. 1996 Feb;22(1): 69-72.
84. Nis¸anci M, Er E, Is¸ik S, Sengezer M. Treatment modalities for post-burn axillary contractures and the versatility of the scapular flap. Burns. 2002 Mar;28(2):177-80. 85. Herndon DN. Total burn care: expert consult. 4th ed: Elsevier; 2012.
86. Johnson JT. Atypical myositis ossificans. J Bone Joint Surg Am. 1957 Jan;39(1):189-93.
98. Ellis M, Frank HG. Myositis ossificans traumatica: with special reference to the quadriceps femoris muscle. J Trauma. 1966 Nov;6(6):724-38.
107. Ahrengart L, Lindgren U, Reinholt FP. Comparative study of the effects of radiation, indomethacin, prednisolone, and ethane-1hydroxy-1,1-diphosphonate (EHDP) in the prevention of ectopic bone formation. Clin Orthop Relat Res. 1988 Apr;(229):265-73. 108. Chao EK, Chen AC, Lee MS, Ueng SW. Surgical approaches for nonneurogenic elbow heterotopic ossification with ulnar neuropathy. J Trauma. 2002 Nov;53(5):928-33. 109. Summerfield SL, DiGiovanni C, Weiss AP. Heterotopic ossification of the elbow. J Shoulder Elbow Surg. 1997 May-Jun;6(3): 321-32. 110. Furman R, Nicholas JJ, Jivoff L. Elevation of the serum alkaline phosphatase coincident with ectopic-bone formation in paraplegic patients. J Bone Joint Surg Am. 1970 Sep;52(6): 1131-7.
111. Hsu JD, Sakimura I, Stauffer ES. Heterotopic ossification around the hip joint in spinal cord injured patients. Clin Orthop Relat Res. 1975 Oct;(112):165-9. 112. Tibone J, Sakimura I, Nickel VL, Hsu JD. Heterotopic ossification around the hip in spinal cord-injured patients. A long-term follow-up study. J Bone Joint Surg Am. 1978 Sep;60(6):769-75. 113. Roberts JB, Pankratz DG. The surgical treatment of heterotopic ossification at the elbow following long-term coma. J Bone Joint Surg Am. 1979 Jul;61(5):760-3. 114. Garland DE. A clinical perspective on common forms of acquired heterotopic ossification. Clin Orthop Relat Res. 1991 Feb; (263):13-29.
101. Munster AM, Bruck HM, Johns LA, Von Prince K, Kirkman EM, Remig RL. Heterotopic calcification following burns: a prospective study. J Trauma. 1972 Dec;12(12):1071-4.
A. Radiotherapy as a local treatment option for heterotopic ossifications in patients with spinal cord injury. Spinal Cord. 2000 Jan;38(1):33-6.
102. Snoecx M, De Muynck M, Van Laere M. Association between muscle trauma and heterotopic ossification in spinal cord injured patients: reflections on their causal relationship and the diagnostic value of ultrasonography. Paraplegia. 1995 Aug;33(8):464-8. 103. VanLaeken N, Snelling CF, Meek RN, Warren RJ, Foley B. Heterotopic bone formation in the patient with burn injuries. A retrospective assessment of contributing factors and methods of investigation. J Burn Care Rehabil. 1989 Jul-Aug;10(4):331-5.
88. Pittenger DE. Heterotopic ossification.
105. Elmstedt E, Lindholm TS, Nilsson OS,
Orthop Rev. 1991 Jan;20(1):33-9.
¨ Tornkvist H. Effect of ibuprofen on heterotopic
· VOLUME 2, ISSUE 10 · e4
106. Steidl L, Ditmar R. Soft tissue calcification treated with local and oral magnesium therapy. Magnes Res. 1990 Jun;3(2):113-9.
100. Paterson DC. Myositis ossificans circumscripta. Report of four cases without history of injury. J Bone Joint Surg Br. 1970 May; 52(2):296-301.
Heterotopic ossification. J Am Acad Orthop Surg. 2004 Mar-Apr;12(2):116-25.
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ossification after hip replacement. Acta Orthop Scand. 1985 Feb;56(1):25-7.
115. Baldwin K, Hosalkar HS, Donegan DJ, Rendon N, Ramsey M, Keenan MA. Surgical resection of heterotopic bone about the elbow: an institutional experience with traumatic and neurologic etiologies. J Hand Surg Am. 2011 May;36(5):798-803. Epub 2011 Apr 2.
104. Ritter MA, Sieber JM. Prophylactic indomethacin for the prevention of heterotopic bone formation following total hip arthroplasty. Clin Orthop Relat Res. 1985 Jun;(196):217-25.
87. Kaplan FS, Glaser DL, Hebela N, Shore EM.
|
116. Sautter-Bihl ML, Liebermeister E, Nanassy
117. Coventry MB, Scanlon PW. The use of radiation to discourage ectopic bone. A nineyear study in surgery about the hip. J Bone Joint Surg Am. 1981 Feb;63(2):201-8. 118. Chao ST, Lee SY, Borden LS, Joyce MJ, Krebs VE, Suh JH. External beam radiation helps prevent heterotopic bone formation in patients with a history of heterotopic ossification. J Arthroplasty. 2006 Aug;21(5):731-6. 119. English C, Carmichael KD. Management of fractures in children with thermal injuries. J Pediatr Orthop. 2002 Nov-Dec;22(6):725-8.
120. Cahalane M, Demling RH. Early respiratory abnormalities from smoke inhalation. JAMA. 1984 Feb 10;251(6):771-3.
121. Wright JG, Einhorn TA, Heckman JD. Grades of recommendation. J Bone Joint Surg Am. 2005 Sep;87(9):1909-10.
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